Since PDGF effects diminished as a result of treatment with sunitinib, this lead Bae et al. to the conclusion that the antisenescence effect through H-CM is derived through the PDGF signal pathway. H-CM is also suggested to exhibit different antisenescence activity as compared to L-CM because of its developmental potential and pluripotency (5,6). FGF 2 was then blocked by sunitinib, supporting that FGF 2 is the inducing effect of PDGF -BB in HDFs. After further investigation, SU5402 and sunitinib both inhibited PDGF -BB while only SU5402 inhibited FGF -2, supporting that FGF -2 is the ultimate downstream protein in this pathway.

Since they treated human cells with mESC-CM, they would have to utilize human stem cells to exhibit the same effects produced within this article. With that in mind, there has been research to suggest that human stem cells should exhibit similar effects through PDGF and FGF for this to be utilized in therapeutics for mediation of ageing and age-related diseases (7) with the methods of this article, supporting that ESCs can be used to mediate the PDGF FGF pathway.